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本文引用的文献

1
Lipoprotein(a) as a potential causal genetic risk factor of cardiovascular disease: a rationale for increased efforts to understand its pathophysiology and develop targeted therapies.脂蛋白(a)作为心血管疾病潜在的因果遗传风险因素:增加对其病理生理学理解和开发靶向治疗的努力的理由。
J Am Coll Cardiol. 2012 Aug 21;60(8):716-21. doi: 10.1016/j.jacc.2012.04.038.
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Oxidative Stress-Mediated Brain Dehydroepiandrosterone (DHEA) Formation in Alzheimer's Disease Diagnosis.氧化应激介导的阿尔茨海默病诊断中的脑脱氢表雄酮(DHEA)形成。
Front Endocrinol (Lausanne). 2011 Nov 8;2:69. doi: 10.3389/fendo.2011.00069. eCollection 2011.
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Effects of nitric oxide on the survival and neuritogenesis of cerebellar Purkinje neurons.一氧化氮对小脑浦肯野神经元存活和突起生成的影响。
J Mol Neurosci. 2012 Feb;46(2):336-42. doi: 10.1007/s12031-011-9590-7. Epub 2011 Jul 5.
4
Is hyperhomocysteinemia an Alzheimer's disease (AD) risk factor, an AD marker, or neither?高同型半胱氨酸血症是阿尔茨海默病(AD)的危险因素、标志物,还是两者都不是?
Trends Pharmacol Sci. 2011 Sep;32(9):562-71. doi: 10.1016/j.tips.2011.05.003. Epub 2011 Jun 20.
5
A lead study on oxidative stress-mediated dehydroepiandrosterone formation in serum: the biochemical basis for a diagnosis of Alzheimer's disease.一项关于氧化应激介导的血清脱氢表雄酮形成的主导研究:阿尔茨海默病诊断的生化基础。
J Alzheimers Dis. 2011;24 Suppl 2:5-16. doi: 10.3233/JAD-2011-101941.
6
Risk of dementia associated with elevated plasma homocysteine in a latin american population.拉丁美洲人群中血浆同型半胱氨酸升高与痴呆症的风险
Int J Alzheimers Dis. 2009 Aug 23;2009:632489. doi: 10.4061/2009/632489.
7
Normalization of hyperhomocysteinemia improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer's disease.高同型半胱氨酸血症的正常化可改善阿尔茨海默病转基因小鼠模型的认知缺陷并改善脑淀粉样变性。
FASEB J. 2010 Oct;24(10):3895-902. doi: 10.1096/fj.10-161828. Epub 2010 Jun 2.
8
The cerebrospinal fluid amyloid beta42/40 ratio in the differentiation of Alzheimer's disease from non-Alzheimer's dementia.脑脊液淀粉样蛋白β42/40 比值在阿尔茨海默病与非阿尔茨海默病痴呆的鉴别诊断中的作用。
Curr Alzheimer Res. 2010 Aug;7(5):470-6. doi: 10.2174/156720510791383796.
9
Decreased dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) concentrations in plasma of Alzheimer's disease (AD) patients.阿尔茨海默病(AD)患者血浆中脱氢表雄酮(DHEA)和硫酸脱氢表雄酮(DHEAS)浓度降低。
Arch Gerontol Geriatr. 2010 Jul-Aug;51(1):e16-8. doi: 10.1016/j.archger.2009.07.001. Epub 2009 Aug 8.
10
Neurobiological and neuropsychiatric effects of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS).脱氢表雄酮(DHEA)和硫酸脱氢表雄酮(DHEAS)的神经生物学及神经精神效应。
Front Neuroendocrinol. 2009 Jan;30(1):65-91. doi: 10.1016/j.yfrne.2008.11.002. Epub 2008 Dec 3.

阿尔茨海默病和血管性痴呆患者的血清同型半胱氨酸、硫酸脱氢表雄酮和脂蛋白(a)。

Serum Homocysteine, Dehydroepiandrosterone Sulphate and Lipoprotein (a) in Alzheimer's Disease and Vascular Dementia.

机构信息

Department of Biochemistry, Institute of Post Graduate Medical Education and Research, Kolkata, India.

出版信息

Aging Dis. 2013 Mar 7;4(2):57-64. Print 2013 Apr.

PMID:23696950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3659251/
Abstract

Alzheimer's disease (AD) and vascular dementia (VAD) are the major forms of dementia affecting elderly people, in which the levels of many metabolites are altered in cerebrospinal fluid (CSF) and serum. These metabolites could be risk factors or potential biomarkers, but the significance of some of these are not clearly understood in the context of the disease pathogenesis. In the present study serum levels of homocysteine, dehydroepiandrosterone sulphate (DHEA-S) and lipoprotein (a) or Lp(a) have been measured by ELISA using commercial kits in AD (n = 40), VAD (n = 40) and age matched control subjects (n = 40). The data are compared by ANOVA and post-hoc analysis. The serum homocysteine is markedly elevated compared to control both in AD and VAD subjects, but to a significantly higher extent in the latter. Lp(a) is increased in the serum of VAD subjects only compared to control. Likewise, serum DHEA-S level is lowered in AD but not in VAD compared to control. The analysis of the present data and those published by others suggest that alterations in homocysteine and Lp(a) in serum are indicators of vascular pathology in AD or VAD, while the lowering of serum DHEA-S is a consequence of AD pathology.

摘要

阿尔茨海默病(AD)和血管性痴呆(VAD)是影响老年人的主要痴呆形式,其中脑脊液(CSF)和血清中的许多代谢物水平发生改变。这些代谢物可能是风险因素或潜在的生物标志物,但在疾病发病机制的背景下,其中一些的意义尚不清楚。在本研究中,使用商业试剂盒通过 ELISA 测量了 AD(n = 40)、VAD(n = 40)和年龄匹配的对照组(n = 40)患者血清中的同型半胱氨酸、脱氢表雄酮硫酸酯(DHEA-S)和脂蛋白(a)或 Lp(a)的水平。通过方差分析和事后分析比较数据。与对照组相比,AD 和 VAD 患者的血清同型半胱氨酸明显升高,但在后者中升高更为显著。仅在 VAD 患者的血清中升高 Lp(a)与对照组相比。同样,与对照组相比,AD 患者的血清 DHEA-S 水平降低,但 VAD 患者没有。对目前数据和其他人发表的数据的分析表明,血清同型半胱氨酸和 Lp(a)的改变是 AD 或 VAD 血管病理学的指标,而血清 DHEA-S 的降低是 AD 病理学的结果。